CD4*CD8* thymocytes

Figure 3 Local effects of TGFß.

TGFp mRNA in blood mononuclear cells than patients with relapsing MS. The data support a disease-limiting role for TGFp in MS.

Patients with myasthenia gravis have elevated levels of AChR-reactive TGFp mRNA-expressing blood mononuclear cells. Levels of circulating TGFp mRNA-expressing cells increase after thymectomy. The relevance of TGFp in myasthenia gravis is unclear, but it may have therapeutic potential in this disease.

Elevated TGFp levels have been reported in serum in HIV infection and in cell supernatants after culture of blood mononuclear cells from human immunodeficiency virus (HlV)-infected patients. Levels of TGFp mRNA-expressing mononuclear cells are elevated in HIV-infected patients' blood. TGFp has been identified by immunohistochemistry in brain tissue of patients with the acquired immune deficiency syndrome (AIDS). It has been suggested that TGFp may play an important role in the spread of infection and/or disease progression by amplifying the existing viral load.

Femtogram concentrations of TGFp , suppresses in vitro myelin antigen (MBP, PLP)-induced upregul-ation of IFNy, IL-4, IL-6, TNFa and lymphotoxin, and of perforin, in MS. TGFp also suppresses AChR-induced upregulation of the same proinflammatory cytokines in myasthenia gravis. In contrast, TGFp has no corresponding effects on IL-10 or on TGFp itself. These selective suppressive effects of TGFp, on autoantigen-induced upregulation of proinflammatory cytokines makes TGFp attractive as a potential therapeutic agent in MS and myasthenia gravis.

See also: Cytokines: Cytokine receptors; Experimental autoimmune encephalomyelitis (EAE); Immunosuppression; Mucosal immunity; Oral tolerance.

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